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Bacterial biofilm extracellular polymeric substance (EPS) is a complex, self-produced matrix of biopolymers, including polysaccharides, proteins, extracellular DNA (eDNA), and lipids, that encases bacterial communities (Flemming & Wingender, 2010). It serves as the primary structural scaffold for biofilms, facilitating surface adhesion and providing a protective barrier against environmental stressors, host immune responses, and antimicrobial agents. In clinical settings, EPS is a major contributor to the persistence of chronic infections, such as those found in cystic fibrosis lungs, chronic wounds, and on medical implants, by physically shielding bacteria and sequestering antibiotics (Koo et al., 2017). The matrix also facilitates cell-to-cell communication and horizontal gene transfer among the encased microorganisms. Therapeutic strategies targeting EPS aim to degrade or destabilize this matrix using enzymes like DNases or glycoside hydrolases, or chemical agents like chelators (Tetz et al., 2009). By breaking down the EPS, these treatments enhance the penetration of conventional antibiotics and promote the clearance of the underlying bacterial population. This approach is critical for addressing the high level of antibiotic tolerance associated with biofilm-mediated diseases.
Enzymatic degradation of matrix components (DNA, polysaccharides, proteins) or chemical chelation of stabilizing ions to disrupt the structural integrity of the biofilm, thereby increasing the susceptibility of embedded bacteria to antibiotics and host immune clearance (Koo et al., 2017; Tetz et al., 2009).
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